The acronym PVR is frequently encountered in medicine, creating confusion as it can refer to different measurements, such as Post-Void Residual. However, in cardiology, PVR stands for Pulmonary Vascular Resistance. This precise measurement quantifies the force the right side of the heart must overcome to push blood through the blood vessels in the lungs. This resistance value is a fundamental indicator of the health of the pulmonary circulation and the workload placed upon the right ventricle.
Understanding Pulmonary Vascular Resistance
Pulmonary Vascular Resistance (PVR) is a calculated value reflecting the opposition to blood flow within the pulmonary circulation. The pulmonary circuit is a low-pressure system, offering far less resistance compared to the systemic circulation. A normal pulmonary artery pressure is typically around one-tenth of the pressure found in the main systemic arteries.
To calculate PVR, clinicians apply a modified version of Ohm’s Law, relating pressure, flow, and resistance. The calculation involves measuring the pressure gradient across the lungs and dividing it by the flow rate, known as the Cardiac Output (CO). The formula is PVR = (Mean Pulmonary Artery Pressure [mPAP] – Pulmonary Artery Wedge Pressure [PAWP]) / Cardiac Output.
The resulting value is reported in Wood units (WU) or dynes·sec·cm⁻⁵. A normal PVR is less than or equal to 2.0 Wood units, or approximately 250 dynes·sec·cm⁻⁵. Values above this threshold signify increased narrowing or stiffness of the small pulmonary arteries and arterioles.
When PVR increases, the right ventricle must generate higher pressure to maintain adequate blood flow through the lungs. This increased workload forces the right ventricle to strain and eventually remodel, which can lead to right-sided heart failure. The PVR value is a direct measure of the afterload, or resistance, that the right side of the heart is battling.
The Diagnostic Necessity of PVR Measurement
The precise measurement of PVR is necessary for the diagnosis and classification of pulmonary vascular disease. PVR cannot be accurately estimated using non-invasive methods like echocardiography. The gold standard for obtaining the necessary pressure and flow data is the invasive procedure known as Right Heart Catheterization (RHC).
During an RHC, a specialized catheter is threaded through a vein and advanced into the right atrium, right ventricle, and pulmonary artery. This procedure allows the simultaneous measurement of the mean Pulmonary Artery Pressure, the Pulmonary Artery Wedge Pressure (reflecting left heart pressure), and the Cardiac Output. These three measurements are then used to calculate the PVR.
The PVR value is crucial for confirming and sub-typing Pulmonary Hypertension (PH). A PVR greater than 2 Wood units, combined with an elevated mean Pulmonary Artery Pressure and a normal Pulmonary Artery Wedge Pressure, confirms pre-capillary pulmonary hypertension. This classification indicates that the disease originates within the small vessels of the lung themselves, including Pulmonary Arterial Hypertension.
PVR is an important factor in pre-surgical evaluation, especially for patients considering heart or lung transplantation. If a patient has severely elevated PVR, a newly transplanted lung may overwhelm the high pressure, leading to immediate right ventricle failure. Measuring PVR helps physicians determine the risk of this post-transplant failure, informing the decision on whether a combined heart-lung transplant is necessary. PVR also plays a role in monitoring disease progression and assessing treatment effectiveness.
Modifying Factors and Therapeutic Targets
PVR is a dynamic physiological variable subject to various influences. One potent natural factor is oxygen level; low levels (hypoxia) trigger hypoxic pulmonary vasoconstriction. This mechanism is a localized reflex that narrows the small pulmonary arteries, redirecting blood flow away from poorly ventilated areas.
Prolonged or generalized hypoxia, such as occurs at high altitude or in severe lung disease, leads to widespread vasoconstriction and a sustained increase in PVR. Other metabolic conditions, such as low blood pH (acidosis), can also cause the pulmonary arteries to constrict. PVR is also influenced by lung volume, being lowest when the lungs are at their functional residual capacity.
The ability to therapeutically modify PVR forms the basis of many treatments for pulmonary hypertension. Clinicians use targeted medications, primarily pulmonary vasodilators, to relax the smooth muscle in the pulmonary arterial walls and lower resistance. These agents include powerful vasodilators like prostacyclin analogues, and phosphodiesterase-5 inhibitors (such as sildenafil), which promote vessel relaxation.
During a diagnostic RHC, vasoreactivity testing may be performed by administering short-acting vasodilating agents like inhaled nitric oxide. If PVR decreases significantly in response, it suggests the patient has a reversible component to their disease. Such patients may be candidates for long-term treatment with oral calcium channel blockers, guiding the selection of medical therapy aimed at reducing PVR.